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Propofol protects human keratinocytes from oxidative stress via autophagy expression

Journal of Dental Anesthesia and Pain Medicine 2017³â 17±Ç 1È£ p.21 ~ 28
À±Áö¿µ, Jeon Hyun-Ook, ±èÀºÁ¤, ±èöȫ, À±Áö¿í, ¹ÚºÀ¼ö, À¯¼öºó, °ûÁø¿ø,
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À±Áö¿µ ( Yoon Ji-Young ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
 ( Jeon Hyun-Ook ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
±èÀºÁ¤ ( Kim Eun-Jung ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
±èöȫ ( Kim Cheul-Hong ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
À±Áö¿í ( Yoon Ji-Uk ) - Pusan National University School of Medicine Department of Anesthesiology and Pain Medicine
¹ÚºÀ¼ö ( Park Bong-Soo ) - Pusan National University School of Dentistry Department of Oral Anatomy
À¯¼öºó ( Yu Su-Bin ) - Pusan National University School of Dentistry Department of Oral Anatomy
°ûÁø¿ø ( Kwak Jin-Won ) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine

Abstract


Background: The skin consists of tightly connected keratinocytes, and prevents extensive water loss while simultaneously protecting against the entry of microbial pathogens. Excessive cellular levels of reactive oxygen species can induce cell apoptosis and also damage skin integrity. Propofol (2,6-diisopropylphenol) has antioxidant properties. In this study, we investigated how propofol influences intracellular autophagy and apoptotic cell death induced by oxidative stress in human keratinocytes.

Method: The following groups were used for experimentation: control, cells were incubated under normoxia (5% CO2, 21% O2, and 74% N2) without propofol; hydrogen peroxide (H2O2), cells were exposed to H2O2 (300 ¥ìM) for 2 h; propofol preconditioning (PPC)/H2O2, cells pretreated with propofol (100 ¥ìM) for 2 h were exposed to H2O2; and 3-methyladenine (3-MA)/PPC/H2O2, cells pretreated with 3-MA (1 mM) for 1 h and propofol were exposed to H2O2. Cell viability, apoptosis, and migration capability were evaluated. Relation to autophagy was detected by western blot analysis.

Results: Cell viability decreased significantly in the H2O2 group compared to that in the control group and was improved by propofol preconditioning. Propofol preconditioning effectively decreased H2O2-induced cell apoptosis and increased cell migration. However, pretreatment with 3-MA inhibited the protective effect of propofol on cell apoptosis. Autophagy was activated in the PPC/H2O2 group compared to that in the H2O2 group as demonstrated by western blot analysis and autophagosome staining.

Conclusion: The results suggest that propofol preconditioning induces an endogenous cellular protective effect in human keratinocytes against oxidative stress through the activation of signaling pathways related to autophagy.

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Keratinocytes; Oxidative Stress; Propofol

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